2014-05-15
Extinction learning is an extensively investigated field of research with a general focus on fear conditioning experiments. Scientists at the Biopsychology lab shed more light on context-specific extinction learning under appetitive conditions. Here, extinction learning refers to the cessation of previously reinforced conditioned responding once reinforcement is withheld. To study the context dependency of extinction learning under appetitive conditions, we adopted and modified a within-subject ABA renewal paradigm from Robert Rescorla (Q J Exp Psychol 61: 1793) and performed pharmacological interventions to investigate fundamental neural mechanisms underlying context-dependent extinction learning. More specifically, we transiently inactivated either the nidopallium caudolaterale (NCL, functional equivalent of mammalian prefrontal cortex) or the hippocampus immediately before extinction training with tetrodotoxin. Both structures are core structures for context-specific extinction learning in fear conditioning paradigms. Using an elegantly controlled procedure, we found that both manipulations lead to non-specifically response suppression. Retrieval testing under drug-free conditions showed that subjects did successfully retrieve extinction memory in the context of acquisition but were impaired when tested in the context of extinction. Thus, the present study suggests that both NCL and hippocampus are involved in the consolidation of extinction memory, and that their contribution to extinction is context-specific.
Within a follow-up experiment we currently explore the function of NMDA-receptor in the NCL for extinction learning.
Extinction learning is an extensively investigated field of research with a general focus on fear conditioning experiments. Scientists at the Biopsychology lab shed more light on context-specific extinction learning under appetitive conditions. Here, extinction learning refers to the cessation of previously reinforced conditioned responding once reinforcement is withheld. To study the context dependency of extinction learning under appetitive conditions, we adopted and modified a within-subject ABA renewal paradigm from Robert Rescorla (Q J Exp Psychol 61: 1793) and performed pharmacological interventions to investigate fundamental neural mechanisms underlying context-dependent extinction learning. More specifically, we transiently inactivated either the nidopallium caudolaterale (NCL, functional equivalent of mammalian prefrontal cortex) or the hippocampus immediately before extinction training with tetrodotoxin. Both structures are core structures for context-specific extinction learning in fear conditioning paradigms. Using an elegantly controlled procedure, we found that both manipulations lead to non-specifically response suppression. Retrieval testing under drug-free conditions showed that subjects did successfully retrieve extinction memory in the context of acquisition but were impaired when tested in the context of extinction. Thus, the present study suggests that both NCL and hippocampus are involved in the consolidation of extinction memory, and that their contribution to extinction is context-specific.
Within a follow-up experiment we currently explore the function of NMDA-receptor in the NCL for extinction learning.